Douglas Webster

Spiral ganglion neuron loss following organ of corti loss: A quantitative study

The packing density of spiral ganglion neurons was measured in 2.5- and 13-15-month-old guinea pigs, in guinea pigs at various times after drug-deafening or acoustic trauma, and in Waltzing guinea pigs of various ages. Analysis of variance and Duncans new multiple range tests were used to determine significant differences between treatment/survival groups. Spiral ganglion neurons in young and old normal ears did not have significantly different packing densities. Drug-deaf guinea pigs showed a significant loss of neurons by 2 weeks following treatment, a further significant loss by 2 months, and a marginally significant loss between 4 and 8 months. The neuronal population was then stable through 15 months, at about 13% of normal. Acoustic trauma ears showed the first significant loss isn the lower second turn at 1 month. Long-term (12-14 months post-exposure) trauma ears were highly variable. Waltzers lost about 50% of their normal neuronal population between 4 and 8 months; they showed an unexpected greater-than-normal density at 2 months, possible explanations of which are discussed. Thus, loss of the organ of Corti from various causes results in a slow but progressive loss of spiral ganglion neurons, the time course of which varies with the type of cochlear insult.

Effects of neonatal conductive hearing loss on brain stem auditory nuclei.

Both postnatal auditory deprivation and experimentally produced conductive hearing losses in mice result in incomplete maturation of most brain stem auditory neurons. The affected groups are: octopus cell, globular cell, small spherical cell, and large spherical cell groups in ventral cochlear nuclei; and the lateral superior olive and medial nucleus of the trapezoid body of the superior olivary complex. When 45 days of auditory deprivation are followed by 45 days of normal acoustic stimulation, there is incomplete maturation of neurons in: multipolar cell, globular cell, small spherical cell, and large spherical cell groups in ventral cochlear nuclei; lateral superior olive and medial nucleus of trapezoid body in superior olivary complex; and central nucleus of inferior colliculus. A critical period exists when adequate sound stimulation is needed for full development of these neurons.

Adaptive Value of Hearing and Vision in Kangaroo Rat Predator Avoidance

The predatory strikes of a sidewinder rattlesnake (Crotalus cerastes) can be avoided by kangaroo rats (Dipodomys merriami) in the normal condition and also after either of two surgical manipulations: (1) removal of the eyes, or (2) reduction of middle ear volume. When both these operations are performed, however, the kangaroo rat is struck by the rattlesnake with relative ease.Reduction of middle ear volume alone in a natural population of kangaroo rats resulted in a high loss of animals with reduced middle ear volume; most of them disappeared from the population during the dark phase of the moon. It is concluded that both vision and audition play significant adaptive roles in predator avoidance.

Projections of the Trapezoid Body and the Superior Olivary Complex of the Kangaroo Rat (Dipodomys merriami); pp. 322–337

Glass micropipettes filled with 2 M sodium cyanide were used to physiologically locate and iontophoretically damage the nucleus of the trapezoid body (NTB), the medial superior olive (MSO), and the lateral superior olive (LSO). Mechanical lesions were made in the trapezoid body as it leaves the cochlear nuclei. After a 3- to 10-day survival time the projections and terminal degeneration were traced with the Fink-Heimer and Nauta-Gygax stains. The ventral cochlear nucleus (VCN) projects via the trapezoid body to ipsilateral LSO, ipsilateral preolivary nuclei, ipsilateral lateral and a contralateral medial dendritic fields of MSO, and contralateral NTB; there is also a small ipsilateral projection to the ventral nucleus of the lateral lemniscus (VNLL) and the central nucleus of the inferior colliculus (CNIC). Some trapezoid body fibers ascend via the contralateral lateral lemniscus to VNLL, DNLL (dorsal nucleus of the lateral lemniscus), and CNIC. There is no projection from the ventral cochlear nucleus to the ipsilateral NTB and contralateral preolivary nuclei. All portions of NTB project ipsilaterally to LSO (ventral NTB to dorsomedial LSO, dorsal NTB to ventral LSO) and to the retro-olivary nucleus. In two animals with NTB lesions there is also degeneration in the ventromedial portion of the ipsilateral facial nucleus. NTB projects contralaterally by way of the stria of Monakow to the pyramidal and molecular cell layers of the dorsal cochlear nucleus (DCN). The NTB does not project ipsilaterally to MSO, preolivary nuclei, VNLL, DNLL and CNIC. Contralaterally there are no projections to any of the nuclei of the auditory pathway except the DCN. Most MSO projections are ipsilateral. The densest goes by way of the lateral lemniscus to the lateral aspect of the ipsilateral CNIC, terminating throughout its dorsoventral axis. MSO also projects bilaterally to the pyramidal and molecular cell layers of dorsal cochlear nucleus (DCN), and ipsilaterally to the ventral portion of the motor nucleus of V and to the facial nucleus. MSO does not project ipsilaterally to the LSO, NTB, preolivary, VCN and retro-olivary nuclei. On the contralateral side, all structures except the DCN are free of projection patterns from axons originating in the MSO. LSO projects bilaterally to the central and ventral portions of CNIC and to the nuclei of the lateral lemnisci, and ipsilaterally to the large and small spherical cell areas of anterior ventral cochlear nucleus (AVCN) and to all portions of DCN. The LSO does not project ipsilaterally to the NTB, MSO, preolivary and retro-olivary nuclei. On the side opposite, this nucleus does not project to NTB, MSO, retro-olive, VCN, preolivary and LSO. For all lesions regardless of the site, there is no degeneration found rostral to the CNIC. The medial geniculate body or other structures in the diencephalon or cortex are free of any fields of terminal degeneration.

Kangaroo Rat Auditory Thresholds before and after Middle Ear Reduction

Four kangaroo rats were conditioned by shock avoidance and their auditory thresholds determined from 125 through 8,000 Hz. The middle ears were reduced and thresholds re-determined. Normal mean thresh

Ascending and Descending Projections of the Inferior Colliculus in the Kangaroo Rat (Dipodomys merriami)

The ascending and descending pathways from the inferior colliculus were studied in the kangaroo rat ( Dipodomys merriami) using aspiration or electro-lesioning techniques. The ipsila

Cochlear Nerve Projections following Organ of Corti Destruction

Experimental organ of Corti destruction results in (1) secondary loss of all type I spiral ganglion neurons, (2) development of type III spiral ganglion neurons, (3) degeneration of most cochlear nerve myelinated fibers, and (4) terminal degeneration in the ventral and dorsal cochlear nuclei. The first signs of degenerative changes occur by eight days after organ of Corti destruction and degeneration debris remains until 28 weeks after destruction.

Projections of the intraotic ganglion to the medullary nuclei in the tegu lizard, Tupinambis nigropunctatus.

The auditory and vestibular projectionsof the posterior ramus of the statoacoustic nerve were traced using silver degeneration techniques in the tegu lizard, Tupinambis nigropunctatus.

Glycogen Content in the Outer Hair Cells of Kangaroo Rat (D. Spectabilis) Cochlea Prior to and Following Auditory Stimulation

Glycogen content in the organ of Corti of the kangaroo rat, D. spectabilis, is evaluated prior to and following auditory stimulation. PAS positive material is prominent in the outer hair cells, tectorial and basilar membranes, bone, and spiral ganglia. PAS positivity in the outer hair cells is due exclusively to glycogen. Short-term, high intensity stimulation of the kangaroo rats resulted in glycogen diminution in the outer hair cells, accompanied by damage to the organ of Corti in the upper half of the basal turn at frequencies of 1 950 and 3 000 Hz. At 3 000 Hz, the degree of damage increases as the intensity of the stimulus is raised. Long-term exposures at moderately high intensities also show the kangaroo rat to be particularly sensitive to frequencies of 1 950 and 3 000 Hz in the basal and second turns of the cochlea. Glycogen content is diminished, however no cytological damage is apparent.

Histocytochemical pattern of enzyme distribution in cochlea of the kangaroo rat (D. spectabilis) at rest and following auditory stimulation.

The histocytochemical distribution of enzymes in the cochlea of the kangaroo rat, Dipodomys spectabilis, at rest and following auditory stimulation was investigated. At rest, enzyme distribution in D. Apectabilis resembles that previously reported by Webster & Stack (1966, 1968) in D. merriami. Krebs cycle enzymes are prominent in the sensory epithelium, stria vascularis, spiral ligament, and external spiral sulcus. The spatial pattern of general esterase activity is also similar. No increase or decrease of either succinic dehydrogenase or carboxylic esterase activity, as measured by a microscopically visible quantitative change in deposition product, is observed following acoustic stimulation. Injury to the basal and second turns, however, is seen in a few cochleae. The validity of using histochemical methods for the demonstration of fluctuation in enzyme activity is discussed.